The present embodiments relate to determining a damage characteristic value of a kidney.
Treatment-resistant hypertension describes a condition characterized by the inability to achieve a sufficient lowering of systolic blood pressure below 160 mmHg in spite of the, in some cases concurrent, administration of at least three antihypertensive agents, including diuretic. As indicated in W. C. Cushman et al., Journal of Clinical Hypertension, Vol. IV, No. VI, 2002, pp. 393 to 404, this disease affects even 8% of the optimally treated hypertensive patients, with an increasing trend; it therefore represents a very large patient cohort. The consequences of high blood pressure existing over many years may include: arteriosclerosis (atherosclerotic vascular disease); coronary heart disease (narrowing of the coronary blood vessels); myocardial infarction; cardiac insufficiency (chronic heart failure); atrial fibrillation; brain damage or stroke (high blood pressure being the primary risk factor for this); calcification or aneurysms of the aorta with risk of rupture and bleeding; kidney damage and renal failure; and/or eye damage with diminution of visual acuity.
Renal denervation, also known as renal sympathetic denervation, renal nerve ablation, renal denervation, or renal artery denervation, is a relatively new method for successfully lowering blood pressure in the long term. Denervation may be the complete or partial interruption of nerve tracts between an organ and the brain. Renal, from the Latin “ren”, kidney, means “relating to the kidney” or “appertaining to the kidney”. In renal denervation, an instrument known as an ablation catheter (e.g., a radiofrequency current ablation catheter) is typically introduced into the renal artery via an access site in the groin of a patient. A radiofrequency current is emitted, causing nerve fibers extending around the kidney vessel to be ablated, with the result that the corresponding nerve pathways, which in some instances conduct spurious signals from the kidney to the brain and back, are interrupted. The kidney is accordingly decoupled from the sympathetic nervous system.
By this method, it is possible, according to H. Krum, Transcatheter Cardiovascular Therapeutics (TCT) Conference, 2009, Sep. 21-26, 2009, San Francisco, Calif., USA, to achieve a clinically significant reduction in blood pressure of about 30 mmHg on average in approximately 80% of patients. Contrasting with the high success rate of 80%, there remain 20% of patients in whom no reduction in blood pressure may be achieved through renal denervation therapy. The cause for when the treatment works for a patient (e.g., the patient is what is called a “responder”) and when it does not has not been conclusively explained to date. Currently, little to no attention is devoted to the difference between “responders” and “non-responders”, attempts being made instead to treat as many patients as possible. This serves to help the medication-resistant patients, and a more extensive database is generated as a result. Current publications, such as in N. Goulding, A new cure for hypertension—Renal Denervation, The Boolean, 2011, put forward the hypothesis that the success of a renal denervation is dependent on the damage state of the kidney. Currently, this damage state of the kidney is measured by, for example, measuring the protein content in urine and/or blood. The creatinine level in the blood is also determined. However, these measurements only describe the state of damage of the kidney indirectly. Precise knowledge about the renal factors on which the regulation of blood pressure is dependent is so important because the kidney constitutes the primary medium- and long-term regulatory organ, with the short-term regulation being effected primarily by way of baroreceptors. The long-term regulation controls the blood pressure by sending signals via the nerves to the brain, resulting in a change in the total blood volume, the heart rate, and the change in vessel diameters. However, in certain circumstances, or under certain preconditions, the kidney also sends out “spurious” signals that lead to a pathological increase in blood pressure, without this being necessary for the body. The diseased kidney may also be the source of a pathological afferent signal that stimulates the efferent sympathetic activity. In the case of renal denervation, such signals from the kidney are prevented by the corresponding nerve tracks being ablated and thus deactivated. As a result the long-term regulation, which in the pathological case is incorrect, may be switched off, and the body regulates the blood pressure primarily by way of short-term regulation mechanisms, such as the baroreceptors.